1. Field of the Invention
The present invention relates generally to implantable cardiac devices, such as implantable cardiac defibrillators (ICDs). The present invention more particularly relates to increasing power efficiency for pacing pulses in such implantable cardiac devices.
2. Background Art
Implantable cardiac stimulation devices, such as implantable cardiac defibrillators (ICDs), are well known in the art. Such devices may include, for example, implantable cardiac pacemakers and defibrillators either alone or combined in a common enclosure. The devices are generally surgically implanted in a pectoral region of the chest beneath the skin of a patient. The primary components of an ICD include a monitoring and detection mechanism, a capacitor, a battery, a sensing system for detecting an arrhythmia, and a control system for controlling delivery of a capacitive discharge electrical shock in response to a detected arrhythmia. The implantable devices generally function in association with one or more electrode carrying leads which are implanted within the heart. The electrodes are positioned within the heart for making electrical contact with the muscle tissue of their respective heart chamber. Conductors within the leads couple the electrodes to the device to enable the device to deliver the desired electrical therapy.
ICDs are often employed to monitor a patient's heart to detect arrhythmias, which are irregular heartbeats that feature either very rapid ventricular contractions due to an abnormally rapid heart rate of about 100–240 beats per minute (tachycardia), an excessively slow heartbeat fewer than 50 to 60 beats per minute (bradycardia) or, most commonly, extra or “premature” beats. The most common arrhythmia is atrial fibrillation, which is an abnormal rhythm of the heart (a rapid, chaotic heart rhythm resulting in no effective pumping of blood) that can result in an increased risk of stroke due to the formation of emboli (blood clots) in the heart. More specifically, atrial fibrillation is an abnormality of heart rhythm in which chambers of the heart no longer contract in an organized manner. Heart rate often becomes irregular and may be very fast, producing palpitations. Atrial fibrillation can lead to symptoms of heart failure (shortness of breath, edema, palpitations) and chest pains and, when left untreated, occasionally can lead to stroke.
The heart has a right side and a left side. Each side has a chamber that receives blood returning to the heart (an atrium) and a muscular chamber that is responsible for pumping blood out of the heart (a ventricle). Atria are relatively thin-walled chambers, whereas the ventricles are much more muscular. Blood passes from the atria into the ventricles through two processes. During the resting phase, when the ventricles are not contracting, the tricuspid and mitral valves open. Some of the blood that has accumulated in the atria passively flows through the tricuspid and mitral valves into the right and left ventricles, respectively. The atria then contract, pumping blood out and into the ventricles. Once the ventricles fill with blood, they contract, pumping blood out of the ventricles, into the lungs, and to the body.
Contractions of the different chambers of the heart are normally organized in a specific manner. An electrical impulse travels through the heart's chambers and sets off contractions. The heart's “spark plug” is a small area of specialized heart tissue called the SA node, located in the right atrium. Each time this tissue “fires,” an impulse travels first through the right and left atria, signaling these chambers to contract and pump blood into the ventricles, and then travels down into a patch of another specialized heart tissue located between the atria and the ventricles, called the AV node. Electrical-wire-like specialized tissue conducts the impulse down into the ventricles, where it signals the right ventricle to contract and to pump blood out and into the lungs, and signals the left ventricle to contract and pump blood out to the rest of the body. Normal sequence of electrical activation of the chambers of the heart is called normal sinus rhythm.
In atrial fibrillation, normal sinus rhythm does not occur. Instead, multiple “wavelets” of electrical impulses travel randomly through the atria, leading to more or less random activation of different parts of the atria at different times. Because the tissues of the right and left atria are not stimulated to contract in an organized manner, the walls of the atria more or less quiver.
Lack of organized contraction by the atria causes several detrimental things to happen. First, because less blood is pumped into the ventricles, there is less blood circulating throughout the body and blood accumulates in the lungs, causing shortness of breath (dyspnea) and other symptoms of heart failure. Second, because the heart is no longer pumping blood into the ventricles, the blood in the atria (particularly in a small part of the left atrium, the left atrial appendage) becomes relatively stagnant. There is a small but real risk that, over time, the stagnant blood will form a blood clot. If a blood clot forms, it may eventually enter the left ventricle and then get pumped out into the body. If this happens, the clot may travel to the brain, block the flow of blood in a cerebral artery, and cause a stroke.
Third, atrial fibrillation can create chest pain (angina). Multiple disorganized wavelets of electrical activity bombard the AV node with electrical impulses. When a great many electrical impulses are conducted through the AV node down into the ventricles, the ventricles contract very rapidly, producing a very fast heart rate. When the ventricles contract too rapidly, less blood is pumped into the body and blood may “back up” into the lungs. Rapid contraction increases the ventricles' demand for oxygen. The demand may exceed the ability of the coronary arteries to supply the ventricles with oxygen-rich blood, causing angina.
When an ICD detects an arrhythmia (e.g., due to atrial fibrillation), the ICD is often used to deliver an appropriate shock to the patient's heart in an attempt to return the heart to normal sinus rhythm. Sometimes, second, third, and fourth (and possibly more) shocks are required in a critical case to return the heart to normal sinus rhythm.
Current ICDs are battery powered. The battery is implanted in the patient as part of the ICD. The types of batteries used in ICDs vary. Typical ICD batteries supply voltage in the range of 2.8 to 3.2 Volts (V), depending on the battery chemistry. In conventional devices, pacing pulses are regulated by a charge pump circuit that multiplies the battery voltage by an integer multiplication factor (e.g., 1X, 2X, 3X, etc.) to obtain the desired pacing voltage.
In many cases, conventional charge pump systems are not power efficient. For example, with modern advances on the pacing leads and auto-capture system, the required pacing voltages have been significantly reduced (usually to less than 1V). If a 0.7V pacing voltage is needed, it will be directly regulated from the battery. If the battery voltage is 2.8V, the efficiency will be 25%. If the battery voltage is 3.2V, the efficiency will be even lower, on the order of 22%. Similarly, if a 3V pacing voltage is required from a 2.8V battery, the conventional charge pump must use a 2×multiplication factor to increase the battery voltage, resulting in a 54% power efficiency.
Methods and devices are therefore needed to increase power efficiency for the pacing pulses.